G268D | shi-PA; G268D | shi-PB; G268D | shi-PC; G268D | shi-PE; G268D | shi-PF; G268D | shi-PG; G268D | shi-PH; G268D | shi-PI; G268D | shi-PJ; G268D | shi-PK; G268D | shi-PL; G268D | shi-PM; G268D | shi-PN; G268D | shi-PO; G268D | shi-PP
Site of mutation reported relative to shi aa sequence.
actin filament & spermatid | conditional ts
adherens junction & wing cell | pupal stage | conditional - heat sensitive
garland cell & endosome
photoreceptor cell & synaptic vesicle
Homozygosity for either PldnΔ1 or Dysbe01028 does not significantly affect the total quanta release during neurotransmission across shi1 homozygous wandering third instar larval neuromuscular junctions at the restrictive 32[o]C temperature.
The abnormal drop in the number of rhodopsin1-containing vesicles (RLVs) observed upon a pulse of bright white light administered to shi1 homozygous adult flies, that have been kept at the permissive temperature of 18[o]C, and followed by a rapid transfer to the non-permissive temperature (25[o]C) is not observed when the shi1 mutant allele is combined with Pld3.1 in homozygous state.
shi1/shi1 does not rescue the bang sensitive phenotype of eas2/eas2 or parabss1/parabss1 mutants at 23[o]C, but if incubated for 3 minutes at 26[o]C or 27[o]C immediately before testing, partially rescues the bang sensitive phenotype of eas2/eas2 or parabss1/parabss1 mutants.
shi1/shi1, eas2/eas2 double mutants exhibit defects in synaptic transmission, as shown by significantly reduced response rate to GF circuit stimulation at 100 Hz; and show seizure-like activity in the DLM and loss of GF circuit responsiveness after temperature shift to 29[o]C.
Boutons in the NMJs of shi1, Syngr1 mutant larvae have an increased synaptic vesicle diameter following a high K[+] shock compared with shi1, SyngrPE controls. The average diameter is comparable to that seen in Syngr1 mutants before K[+] stimulation. The boutons contain a significantly greater number of endocytic cisternae (diameter >200nm) compared with controls. Synaptic vesicle density is reduced compared with controls.
The time taken for shi1 flies to be paralysed on shifting to the restrictive temperature is significantly decreased, while time needed for recovery for these mutants on returning to the permissive temperature is significantly increased in a BicDr5/+ genetic background.
shi1; stmA1 double mutants are synthetically lethal. No double homozygous female third instar larvae can be recovered, indicating that lethality occurs at the second instar stage or earlier. In contrast, shi1/y; stmA1/stmArev499 males can be recovered at third instar at a very low frequency at 16[o[C, before they also die at an early pupal stage.
shi1; stmA1/stmArev499 males exhibit decreased FM1-43 dye loading at the larval neuromuscular junction, compared to controls. However, the double mutant exhibits the same level of loading as in shi1 single mutant males.
Vesicle endocytosis occurs at reduced rates in shi1; stmA1/stmArev499 males at 18[o[C compared to controls, although there is no significant difference between shi1;y and shi1/y; stmA1/stmArev499 mutants.
At the restrictive temperature, evoked release is abolished in shi1; cpxSH1 double mutant animals. The elevated miniature excitatory junctional potential frequency observed at the permissive temperature is eliminated in the double mutant.
shi1; Df(3R)Hsp70A, Df(3R)Hsp70B mutants show a higher sensitivity to pretreatment at 35oC for 30 min followed by 40 min at 38oC than shi1 flies. The double mutants show higher levels of paralysis and fail to recover, even 24 hours after the heat shock.
The formation of holes in wings due to temperature shift of shi1/shi1 animals during pupal stages is mildly enhanced by stan3/+, moderately enhanced by dgo380/+, Vangstbm-6/+ or pk1/+ and strongly enhanced by pksple-1/+ or Vangstbm-D/+.
The F-actin density in the investment cones of spermatid individualization complexes is further decreased following a heat pulse of 11 hours in ctpins1, shi1 and ctpDIIA82, shi1 double mutants compared to shi1 single mutants.
The tracheal system phenotypes of shi1 homozygous embryos (collected at the permissive temperature (25oC) for 7 h and then shifted to 34oC for another 7 hours) are dominantly enhanced by awdj2A4 : the penetrance of the most severe phenotypic class is increased from 1.2% to 33.2% by the presence of awdj2A4/+. (Note, these sever phenotypes are never observed in awdj2A4/+ embryos raised under the same conditions).
Flies with endoAEP927;shi1 eyes suffer a depletion of functional synaptic vesicles when raised to 29oC for 15 minutes to the same extent as flies with single shi1 mutant eyes. After 30 minutes of recovery time at 18oC following the 15 minutes at 29oC, endoAEP927;shi1 photoreceptor terminals show an increased number of capitate projections, which are invaginations of epithelial glia, compared to shi1 single mutants. Additionally, membrane sheets emerging from near the pedestal of the T-bar ribbon of photoreceptor terminals persist for longer during the recovery time in endoAEP927;shi1 double mutants than shi1 single mutants. There is less synaptic vesicle depletion in endoAEP927;shi1 mutant terminals following exposure to 29oC than in shi1 terminals. These vesicles appear clustered and electron dense in the double mutants, similar to their appearance in endoAEP927 single mutants. In endoAEP927;shi1 mutants, free vesicles persist during exposure to 29oC, while in shi1 mutants, vesicles do not remain coated at this temperature.
Rab5N142I.Scer\UAS mutants, expressed with Scer\GAL4hs.PS in shi1 mutants, induces enlargement of vesicles. These vesicles disappear when flies are kept at 30oC (shi1 restrictive temperature). When flies are returned to 20oC (shi1 permissive temperature), enlarged vesicles, along with normal-sized vesicles are re-formed in the terminal.
shi1/Y ; mlenap-ts1/mlenap-ts1 animals have near-normal heartbeats at temperatures from 20-35oC, but have an abnormal heart rate at 37oC. shi1/Y ; mlenap-ts1/+ animals have near-normal heartbeats at temperatures from 25-37oC, but have an abnormal heart rate at 20oC. shi1/shi1 ; mlenap-ts1/mlenap-ts1 animals have significantly slower than normal heart rates at all temperatures but the beat is normally rhythmic. shi1/shi1 ; mlenap-ts1/+ animals have significantly slower and less rhythmic than normal heart rates at several temperatures.
NAx-59b shi1 double mutant clones in the thorax induced during the larval stage at the restrictive temperature present a strong neurogenic phenotype (excess of bristles), at the permissive temperature they are completely devoid of bristles. Homozygous Nl1N-ts1 clones exhibit a strong neurogenic phenotype, all bristles at the border of the clone are mutant. Nl1N-ts1 shi1 clones also exhibit a strong neurogenic phenotype, 7% bristles along the clone border are wild type. Occasionally adjacent wild type and mutant bristles are seen.